Frontal Fibrosing Alopecia: A Review of Disease Pathogenesis
July 2022
in “
Frontiers in Medicine
”
frontal fibrosing alopecia FFA immune cell inflammatory responses histological findings inflammatory cell infiltration immune privilege autoimmune diseases interferon-γ IFN-γ epithelial-mesenchymal transition EMT peroxisome proliferator-activated receptor γ PPAR-γ mammalian target of rapamycin mTOR HLA-B*07:02 sex steroids
![Image of study](/images/research/317d9d93-83c3-4437-9444-923c00975280/medium/15765.jpg)
TLDR The cause of Frontal fibrosing alopecia, a type of hair loss, is complex, likely involving immune responses and genetics, but is not fully understood.
Frontal fibrosing alopecia (FFA) is a type of irreversible hair loss, often seen in postmenopausal women, characterized by a receding frontal and temporoparietal hairline. The pathogenesis of FFA is complex and not fully understood, but it is believed to involve immune cell and substance-mediated inflammatory responses, with histological findings showing inflammatory cell infiltration around lesioned hair follicles. The disease is associated with a collapse of immune privilege in hair follicles and is linked to many autoimmune diseases. Factors such as interferon-γ (IFN-γ), epithelial-mesenchymal transition (EMT), peroxisome proliferator-activated receptor γ (PPAR-γ), and the mammalian target of rapamycin (mTOR) signaling pathway play a role in the disease's progression. Genome-wide association analysis indicates that FFA is an immune inflammatory disease with a genetic predisposition, specifically driven by HLA-B*07:02. The roles of sex steroids and external stimuli in FFA are speculative and derived from clinical studies of disease behavior. More extensive studies are needed to confirm the actual pathogenesis of FFA.